Herpes simplex virus is a human pathogen which can produce recurrent disease via a cycle of latent and lytic infections. To understand the mechanism by which the virus is reactivated from the quiescent state in the sensory ganglia of the host individual, the factors which regulate the expression of the viral immediate early genes have been characterized. Presently, studies focus upon the role of the cellular C1 factor in the modulation of the viral lytic-latent cycle as this protein undergoes a series of regulatory modifications, plays a critical role in the regulation of HSV IE gene expression, and is involved in other basic cellular processes. Using developed antiseras, the C1 factor was shown to undergo a specific activation in sensory neurons which correlates with the reactivation of the virus from the latent state. As there is no tissue culture system which reproduces a viral latent infection, a mouse model system is being developed to analyze the role of the C1 factor in regulating the viral infection cycle. To this end, cDNAs and genomic DNAs have been isolated and characterized which encode the mouse homologue of the human factor. The factor is evolutionarily well conserved and exhibits characteristics similar to the human protein. Significantly, the expression of the C1 factor in mouse and human tissues correlates with the distinct tissue tropism that is exhibited by HSV in these two organisms. The characterization of the mouse C1 factor allows for the continued development of an animal model system for the analysis of the role of this protein in the determination of HSV lytic and latent infections.